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Lipids
A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant and Hackh's Chemical Dictionary, 5th ed)
Year introduced: /blood was BLOOD LIPIDS 1963-1967
Membrane Lipids
Lipids, predominantly phospholipids, cholesterol and small amounts of glycolipids found in membranes including cellular and intracellular membranes. These lipids may be arranged in bilayers in the membranes with integral proteins between the layers and peripheral proteins attached to the outside. Membrane lipids are required for active transport, several enzymatic activities and membrane formation.
Year introduced: 1977
Lipolysis
The metabolic process of breaking down LIPIDS to release FREE FATTY ACIDS, the major oxidative fuel for the body. Lipolysis may involve dietary lipids in the DIGESTIVE TRACT, circulating lipids in the BLOOD, and stored lipids in the ADIPOSE TISSUE or the LIVER. A number of enzymes are involved in such lipid hydrolysis, such as LIPASE and LIPOPROTEIN LIPASE from various tissues.
Year introduced: 1980
Glycation End Products, Advanced
A heterogeneous group of compounds derived from rearrangements, oxidation, and cross-linking reactions that follow from non-enzymatic glycation of amino groups in PROTEINS; LIPIDS; or NUCLEIC ACIDS. Their accumulation in vivo accelerates under hyperglycemic, oxidative, or inflammatory conditions. Heat also accelerates the formation of advanced glycation end products (AGEs) such seen with the browning of food during cooking.
Year introduced: 2018 (1993)
Phospholipids
Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides see GLYCEROPHOSPHOLIPIDS) or sphingosine (SPHINGOLIPIDS). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system.
Year introduced: /metabolism was PHOSPHOLIPID METABOLISM 1965
Lamellar Bodies
Endolysosomal organelles surrounded by multi-lamellar MEMBRANE LIPIDS. They are involved in diverse functions in storage and secretion of cellular LIPIDS. Lamellar bodies in the TYPE 2 PNEUMOCYTES produce and secrete PULMONARY SURFACTANT (e.g., DIPALMITOYL PHOSPHATIDYLCHOLINE). Lamellar bodies in the skin produce and secrete neutral lipids to provide hydrophobic barrier. Pathological accumulation of lamellar bodies are also known in lipid storage diseases (e.g.,LCAT DEFICIENCY; and HERMANSKY-PUDLAK SYNDROME).
Year introduced: 2022
Lipid Droplets
Dynamic cytoplasmic organelles found in almost all cells. They consist of a central core of LIPIDS surrounded by a phospholipid monolayer studded with surface proteins, and are involved in LIPID METABOLISM and storage.
Year introduced: 2015
Dyslipidemias
Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.
Year introduced: 2006
Sphingolipids
A class of membrane lipids that have a polar head and two nonpolar tails. They are composed of one molecule of the long-chain amino alcohol sphingosine (4-sphingenine) or one of its derivatives, one molecule of a long-chain acid, a polar head alcohol and sometimes phosphoric acid in diester linkage at the polar head group. (Lehninger et al, Principles of Biochemistry, 2nd ed)
Year introduced: 1972(1971)
Lipid Mobilization
LIPOLYSIS of stored LIPIDS in the ADIPOSE TISSUE to release FREE FATTY ACIDS. Mobilization of stored lipids is under the regulation of lipolytic signals (CATECHOLAMINES) or anti-lipolytic signals (INSULIN) via their actions on the hormone-sensitive LIPASE. This concept does not include lipid transport.
Year introduced: 1970
Fat Emulsions, Intravenous
Emulsions of fats or lipids used primarily in parenteral feeding.
Year introduced: 1979
MLN64 protein, mouse [Supplementary Concept]
mice homozygous for the Mln64 mutant were viable, neurologically intact,and fertile. No significant changes in plasma lipids, liver lipids, or expression of genes involved in sterol metabolism were observed, except for an increase in sterol ester storage
Date introduced: June 7, 2004
viral envelope lipids [Supplementary Concept]
lipids present in viral envelopes
Date introduced: December 15, 1986
Lipid Accumulation Product
An index for monitoring the accumulation of lipids based on the WAIST CIRCUMFERENCE measurement and the level of TRIGLYCERIDES circulating in the blood.
Year introduced: 2014
Parenteral Nutrition Solutions
Specialized solutions for PARENTERAL NUTRITION. They may contain a variety of MICRONUTRIENTS; VITAMINS; AMINO ACIDS; CARBOHYDRATES; LIPIDS; and SALTS.
Year introduced: 2011
Lipid Regulating Agents
Substances that alter the metabolism of LIPIDS.
Lipoylation
Covalent attachment of LIPIDS and FATTY ACIDS to other compounds and PROTEINS.
Year introduced: 2008
Chylomicron Remnants
Metabolic products of chylomicron particles in which TRIGLYCERIDES have been selectively removed by the LIPOPROTEIN LIPASE. These remnants carry dietary lipids in the blood and are cholesterol-rich. Their interactions with MACROPHAGES; ENDOTHELIAL CELLS; and SMOOTH MUSCLE CELLS in the artery wall can lead to ATHEROSCLEROSIS.
Year introduced: 2007 (2000)
Apoprotein(a)
A large and highly glycosylated protein constituent of LIPOPROTEIN (A). It has very little affinity for lipids but forms disulfide-linkage to APOLIPOPROTEIN B-100. Apoprotein(a) has SERINE PROTEINASE activity and can be of varying sizes from 400- to 800-kDa. It is homologous to PLASMINOGEN and is known to modulate THROMBOSIS and FIBRINOLYSIS.
Year introduced: 2007 (1986)
Multiple Sulfatase Deficiency Disease
An inherited metabolic disorder characterized by the intralysosomal accumulation of sulfur-containing lipids (sulfatides) and MUCOPOLYSACCHARIDES. Excess levels of both substrates are present in urine. This is a disorder of multiple sulfatase (arylsulfatases A, B, and C) deficiency which is caused by the mutation of sulfatase-modifying factor-1. Neurological deterioration is rapid.
Year introduced: 2007